1. Field of the Invention
The present invention is directed to a method and apparatus for heart therapy of the type wherein a pulsed stimulation current is supplied to a physiological representative of the parasympathetic nerve in order to activate same in response to a detection of an impending (incipient) or established arrhythmia.
2. Description of the Prior Art
A modern, automatic, implantable defibrillator, e.g. as described in Current Problems in Cardiology, Volume XIV, No. 12, Dec. 1989, Chicago, Troup J. P. "Implantable Cardioverters and Defibrillators", pp. 699-700, includes cardioversion and pacemaker stimulation options, for both tachycardia and bradycardia in addition to the defibrillation function and is sometimes referred to as an AICD (automatic implantable cardioverter defibrillator). In AICD defibrillation, an attempt is made to induce all heart cells to depolarize simultaneously by applying a strong electrical field across the heart, i.e. The heart is given an electrical shock. The electrical shock is in the form of electrical pulses which can sometimes be delivered in more or less sophisticated spatial and chronological patterns.
Considerable electrical energy (5-40 J) is required for defibrillation, and thus tissue subjected to the shock could be damaged. For this and other reasons, attempts are being made to reduce the electrical energy needed for defibrillation. Within the scope of the ACID prior art, a radical reduction in energy, i.e. a reduction on the order of a factor of ten or more, is actually only possible, in the event of an arrhythmia such as tachycardia, which sometimes appears prior to a fibrillation episode, when the therapeutic device operates with ATP (anti-tachycardia pacing). With ATP, pacing pulses are emitted in relation to the tachycardia beats in a pattern causing the pacing pulses to terminate the tachycardia. There, the energy of the pacing pulses in ATP is of the same magnitude as for conventional pacing pulses for bradycardia, i.e. on the order of microjoules. The ATP technique, however, is only applicable to a tachycardia which may precede the fibrillation episode, and cannot replace defibrillation of a heart exhibiting established ventricular fibrillation.
In therapy in the form of electrical nerve stimulation for treating disorders others than those occurring in the heart in tachyarrhythmias, it has long been known that the energy required is very small, as in pacemaker treatment of the heart, compared to the above-described conventional levels in defibrillation.
Electrical nerve stimulation and the energy needed therefor can be achieved with a modern system for stimulation of the vagus nerve in the treatment of epilepsy, as described in an article by Tarver et al.: "Clinical Experience with Helical Bipolar Stimulating Lead", Pace, Vol. 15, October, Part II 1992, This system employs a pulse generator which is subcutaneously implanted in the upper left part of the thorax region and which is connected to a nerve-stimulating electrode arranged around the left vagus nerve in the nec area. During nerve stimulation, the generator emits 0-12 mA pulses with a pulse width of 130 to 1000 microseconds.
A heart therapy device based on electrical nerve stimulation may thus be one way of addressing the problem of the high levels of energy needed in conventional AICD techniques. The heart's innervation will now be briefly described in order to provide an explanation of the way such a heart therapy device could be achieved.
The vagus nerve is also of interest as regards the heart and the action of the nervous system thereon, since this nerve forms a part of the autonomic nerve system. The autonomic nerve system innervates the heart in the form of two sub-system, the sympathetic and the parasympathetic. From the physiological point of view, these systems are represented by a number of nerves or nerve strings (with attendant ganglia) in different locations. The terms "sympathetic nerve", and "vagus nerve" will often be used below, for simplicity, for the two sub-systems and attendant nerves/nerve strings, despite the actual complexity of innervation. Details will, however, be provided in the description when needed for the understanding. Increased signal activity in the sympathetic nerve increases heart activity (heart rate and stroke volume), whereas increased signal activity in the vagus nerve reduces heart activity (heart rate). Activity in the sympathetic nerve and the vagus nerve normally balance each other so that the heart maintains an appropriate rate at rest of about 70 beats/minute.
Partly in view of the above considerations, activating electrical stimulation of the vagus nerve for prophylaxis and treatment of both ventricular and supraventricular arrhythmias has recently been proposed (Max Schaldach "Electrotherapy of the heart", 1992, Springer Verlag Heidelberg, pp. 210-214). As described therein, the increased activity in the sympathetic nerve in the case of impending or established tachyarrythmia is monitored by intraventricular measurement of impedance, i.e. by indirect measurement of sympathetic activity, in order to control the emission of activating electrical pulses to the vagus nerve during impending or established tachyarrythmia.
The present inventors, in their own animal experiments and measurements concerning tachyarrhythmias encompassing fibrillation, were unable to find any defibrillation effect arising from stimulation of the vagus nerve during established, ventricular fibrillation.